1. Field
The present disclosure relates to a composition for reducing cellular senescence, a method of reducing cellular senescence in a mammal, and a method of treating a symptom associated with cellular senescence in a mammal.
2. Description of the Related Art
Senescence may be defined as a permanent halt in cell division. Replicative senescence or cellular senescence is observed as a model for aging at a cellular level. When cells are consecutively cultured, the cells are divided a number of times, but the cells are no longer divided according to cellular aging. The senescent cells actually have resistibility to programmed cell death, and in some cases, the senescent cells are maintained in a non-dividing state for years.
Ataxia telangiectasia mutated (ATM) is a serine/threonine protein kinase that is recruited and activated by DNA double-strand breaks. The ATM phosphorylates several key proteins that initiate activation of a DNA damage checkpoint, leading to cell cycle arrest, DNA repair, or cellular apoptosis. Several of these targets, including p53, CHK2, and H2AX, are tumor suppressors. The protein is named for the disorder ataxia telangiectasia caused by mutations of the ATM. The ATM belongs to the superfamily of phosphatidylinositol 3-kinase-related kinases (PIKKs). The PIKK superfamily includes six serine/threonine protein kinases that show a sequence similarity to a phosphatidylinositol 3-kinase (PI3K).
There remains a demand for a composition and a method for reducing cellular senescence.